Collaborating genomic, transcriptomic and microbiomic alterations lead to canine extreme intestinal polyposis.

ABSTRACT: Extreme intestinal polyposis in pet dogs has not yet been reported in literature. We identified a dog patient who developed numerous intestinal polyps, with the severity resembling human classic familial adenomatous polyposis (FAP), except the jejunum-ileum junction being the most polyp-dense. We investigated this dog, in comparison with 22 other dogs with spontaneous intestinal tumors but no severe polyposis, and with numerous published human cancers. We found, not APC mutation, but three other alteration pathways as likely reasons of this canine extreme polyposis. First, somatic truncation mutation W411X of FBXW7, a component of an E3 ubiquitin ligase, over-activates MYC and cell cycle-promoting network, accelerating crypt cell proliferation. Second, genes of protein trafficking a

SUBMITTER: Wang J 

PROVIDER: S-EPMC6044369 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature